Chronic administration of methylphenidate induces lipid peroxidation in the striatum of young rats
Noropsikiyatri Arsivi, cilt.46, sa.4, ss.163-168, 2009 (Scopus, TRDizin)
- Yayın Türü: Makale / Tam Makale
- Cilt numarası: 46 Sayı: 4
- Basım Tarihi: 2009
- Dergi Adı: Noropsikiyatri Arsivi
- Derginin Tarandığı İndeksler: Scopus, TR DİZİN (ULAKBİM)
- Sayfa Sayıları: ss.163-168
- Anahtar Kelimeler: Methylphenidate, lipid peroxidation, oxidative stress, striatum, adverse effects
- Sağlık Bilimleri Üniversitesi Adresli: Evet
Özet
Objective: Methylphenidate is the most commonly prescribed psychostimulant and is indicated in the treatment of attention-deficit hyperactivity disorder. There have been concerns about potential adverse effects of long-term methylphenidate administration on the brain. The purpose of this study is to investigate antioxidant system and lipid peroxidation in order to evaluate the potential adverse effects of methylphenidate on the brain. Methods: Methylphenidate at doses of 2 mg/kg (n=10) and 10 mg/kg (n=10) via gavage was administered to young Wistar rats (n=10) for 5 weeks, whereas the controls (n=10) were given saline solution. Methylphenidate and saline solution were given orally and twice daily to match human medication. Superoxide dismutase, glutathione peroxidase, and malondialdehyde were measured in hippocampus, cerebellum, striatum, and frontal cortex of rat brains. Results: Methylphenidate at doses of 2 mg/kg and 10 mg/kg increased the levels of malondialdehyde in the striatum compared to the control group (p<0.01). At a dose of 10 mg/kg, methylphenidate decreased the superoxide dismutase activity in the frontal cortex compared to 2 mg/kg methylphenidate (p<0.05). However, there was no effect on glutathione peroxidase activity. Discussion: The present study suggests that at doses of both 2 mg/kg and 10 mg/kg, the long-term methylphenidate treatment causes lipid peroxidation in the striatum of rat brain. Future studies should be conducted to examine whether antioxidant supplementation can prevent the brain tissue from methylphenidate induced oxidative stress. © Archives of Neuropsychiatry, published by Galenos Publishing. All rights reserved.